![]() Laboratory analysis revealed hypochromic microcytic anaemia (haemoglobin (Hb) 11.5 g/dl (mean corpuscular haemoglobin (MCH) 25.3 pg, mean corpuscular volume (MCV) 75.4 fl), normal values for white blood count, liver and kidney parameters, electrolyte status, total protein and TSH. Due to the broken hip joint prosthesis with chronic pain symptoms, another revision surgery followed 1 month before presentation with a change to a ceramic-ceramic bearing couple, this time a Delta ceramic (in 2011 it was still Forte ceramic) (Fig. Because of a broken ceramic head, revision surgery of the right hip was accomplished in 2012 with a metal head/polyethylene (PE) bearing couple. Prior to this condition, the patient had not been diagnosed with any chronic disease.ĭue to coxarthrosis on the right side, a total hip arthroplasty (H-TEP) with ceramic-ceramic bearing couple (KER/KER-H-TEP) had been performed in 2011. Because of these serious health limitations, he had to give up his business. Myocarditis and hyperacusis had already been diagnosed three years earlier, as well as hypothyroidism 2 years earlier and optic nerve atrophy in the last year. In March 2018, a 63-year-old Caucasian male patient (BMI 27.7 kg/m 2) with fatigue, decreased vision and hearing, metallic taste, difficulty falling asleep, nocturnal urination, hand tingling paraesthesia and numbness in the feet for 3 years presented to our medical facility for further diagnosis and treatment. What is unique about this case report is the description of the long-term follow-up of clinical symptoms associated with the in vivo toxicology of cobalt and chromium in urine and plasma without chelation therapy. Additionally, there is little experience with potential chelation therapies such as EDTA (ethylene diamine tetraacetic acid) or BAL/DMPS (dimercaprol/2,3 dimercapto-1-propanesulfonic acid), whose efficacy has been judged unclear even in the presence of good renal function. Little is known about the toxicological excretion kinetics of cobalt and chromium and their clinical course over several years. Metallic abrasion of damaged prosthetic material causes the release of cobalt ions, which accumulate in the tissue and can lead to multiple toxic organ damage via systemic distribution in the blood. To date, only one case has been published with severe cobalt intoxication above 600 μg/L, also following a hip prosthesis fracture. The reference value of the blood cobalt concentration is 0.45 μg/L. Typical diseases of cobalt intoxication are cardiomyopathy, hypothyroidism and neurological impairments with polyneuropathy, visual and hearing loss. Isolated case reports of symptomatic cobalt intoxication after broken ceramic–metal and metal–metal hip joint endoprosthesis have been described since the early 2000s. ![]() ![]() However, due to the continuous release of metal ions from the tissue, complete recovery did not occur. Specific symptoms such as cardiomyopathy and neurological symptoms were declining. After the elimination of the source of poisoning, the long-term course showed constant excretion of cobalt and chromium over several years without chelation. The patient’s ordeal could have been much shorter if his cobalt intoxication with neurologic, cardiac and thyroid symptoms had been detected earlier by toxicological blood tests. The intoxication was not diagnosed until 6 years after the faulty hip joint revision and 3 years of clear signs of intoxication during a 2nd revision of the prosthesis. Close clinical and toxicological monitoring was performed. Because the blood cobalt concentration decreased rapidly after surgery and symptoms improved, chelation therapy was not applied. Blood analyses showed a cobalt concentration of 600 μg/L (reference value < 0.45 μg/L). He presented 1 month after 2nd revision surgery of a broken hip endoprosthesis in a reduced general condition with signs of heart failure, pale skin and diminished hearing and vision. We report here a 63-year-old male Caucasian with severe cobalt and chromium intoxication. This case report shows the long-term course of complications caused by cobalt and chromium exposure after substantial elimination of the source of intoxication. Less is known about long-term progression of these pathologies. Typical symptoms include cardiomyopathy, neurological symptoms with visual and hearing loss and hypothyroidism. ![]() Cobalt intoxications from fractured hip endoprostheses have been described since the early 2000s.
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